Huntington's disease (HD) is a genetic and fatal neurodegenerative disease characterized by early metabolic dysfunction and psychiatric disturbances such as depression and anxiety. The underlying neurobiological mechanisms for these clinical aspects of the disease are not known but would likely serve as critical targets for disease-modifying treatments once identified. We have previously established a link between hypothalamic mutant huntingtin (mhtt) expression and metabolic dysfunction in HD. Using adeno-associated viral vectors, hypothalamic inactivation of mutant htt in the BACHD mouse model, which expresses the full-length human mhtt, prevented the development of metabolic as well as depressive-like behaviors, thus implicating the importance of an intact hypothalamic neuroendocrine circuitry for HD. However, precisely when the dysfunctional psychiatric phenotype develops has yet to be established. Our work now focuses on the further characterization of the developmental profile of the psychiatric impairments (anxiety- and depressive-like behaviors) by conducting a systematic analysis using a battery of behavioral tests on adult BACHD mice at 4, 12 and 18 months of age across both genotype and gender. Besides the classical behavioral tests, isolation-induced ultrasonic vocalizations were also measured in pups at P0, P5 and P10 across both genotype and gender as a measure of potential early anxiety-like behaviors. We show that the BACHD mice exhibited early signs of anxiety and depressive-like behaviors which become progressively abated with age. Together, these observations provide novel information about non-motor behaviors in this mouse model which could aid in determining the critical therapeutic window for disease-modifying treatments for HD.